Journal
NEUROBIOLOGY OF LEARNING AND MEMORY
Volume 89, Issue 3, Pages 212-218Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nlm.2007.08.008
Keywords
protein synthesis inhibitor; anisomycin; cycloheximide; gene superinduction; memory; consolidation; reconsolidation; extinction
Funding
- NIMH NIH HHS [R01 MH073669, R01 MH073669-01A2, R01 MH073669-02, MH073669] Funding Source: Medline
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To date, the effects of protein synthesis inhibitors (PSI) in learning and memory processes have been attributed to translational arrest and consequent inhibition of de novo protein synthesis. Here we argue that amnesia produced by PSI can be the direct result of their abnormal induction of mRNA-a process termed gene superinduction. This action exerted by PSI involves an abundant and prolonged accumulation of mRNA transcripts of genes that are normally transiently induced. We summarize experimental evidence for the multiple mechanisms and signaling pathways mediating gene superinduction and consider its relevance for PSI-induced amnesia. This mechanistic alternative to protein synthesis inhibition is compared to models of electroconvulsive seizures and fragile x syndrome associated with enhanced mRNA/protein levels and cognitive deficits. (C) 2007 Elsevier Inc. All rights reserved.
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